Chronic heart failure is often characterized by cardiac muscle cell contractile dysfunction, which is likely caused by alterations in heart muscle cell gene expression. Studies with cultured heart muscle cells have revealed fundamental differences in the gene expression programs leading to several different types of heart muscle cell failure. One common type of heart muscle failure has been associated with alterations in genes regulating hormone receptor function. In the failing human heart, there is a reduction in the number of a specific hormone receptor, designated the beta1-adrenergic receptor, and signaling failure normally mediated through a second receptor, designated the beta2-adrenergic receptor. These changes may serve to protect heart muscle cells, but they also diminish the ability of the heart muscle pump to respond to normal factors that would improve contractility in times of physical stress. Revolutionary studies performed by Dr. Gilbert and his associate, Dr. Bristow (now at the University of Colorado), demonstrated that treating heart failure with drugs that block the activity of b-adrenergic receptors leads to improvement in function of the heart pump. This study is designed to test the effects of a b-adrenergic receptor-blocking drug (dobutamine) and a drug that disrupts signaling events mediated through the b-adrenergic receptor (the phosphodiesterase inhibitor, milrinone) in an effort to dissect the complex mechanisms involved as heart muscle cells develop abnormalities of contraction in patients who develop heart failure.